Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging

Before the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive disor...

Full description

Bibliographic Details
Main Authors: Zoey K. Wallis, Kenneth C. Williams
Format: Article
Language:English
Published: MDPI AG 2022-02-01
Series:Viruses
Subjects:
Online Access:https://www.mdpi.com/1999-4915/14/2/409
_version_ 1827652151838507008
author Zoey K. Wallis
Kenneth C. Williams
author_facet Zoey K. Wallis
Kenneth C. Williams
author_sort Zoey K. Wallis
collection DOAJ
description Before the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive disorders, lung and kidney disease, and malignancies. The broad evidence suggests that HIV with ART is associated with accentuated aging, and that the age-related comorbidities occur earlier, due in part to chronic immune activation, co-infections, and possibly the effects of ART alone. Normally the immune system undergoes alterations of lymphocyte and monocyte populations with aging, that include diminished naïve T- and B-lymphocyte numbers, a reliance on memory lymphocytes, and a skewed production of myeloid cells leading to age-related inflammation, termed “inflamm-aging”. Specifically, absolute numbers and relative proportions of monocytes and monocyte subpopulations are skewed with age along with myeloid mitochondrial dysfunction, resulting in increased accumulation of reactive oxygen species (ROS). Additionally, an increase in biomarkers of myeloid activation (IL-6, sCD14, and sCD163) occurs with chronic HIV infection and with age, and may contribute to immunosenescence. Chronic HIV infection accelerates aging; meanwhile, ART treatment may slow age-related acceleration, but is not sufficient to stop aging or age-related comorbidities. Overall, a better understanding of the mechanisms behind accentuated aging with HIV and the effects of myeloid activation and turnover is needed for future therapies.
first_indexed 2024-03-09T20:51:32Z
format Article
id doaj.art-607e15b155594e97b8d775a6e140fb96
institution Directory Open Access Journal
issn 1999-4915
language English
last_indexed 2024-03-09T20:51:32Z
publishDate 2022-02-01
publisher MDPI AG
record_format Article
series Viruses
spelling doaj.art-607e15b155594e97b8d775a6e140fb962023-11-23T22:32:26ZengMDPI AGViruses1999-49152022-02-0114240910.3390/v14020409Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated AgingZoey K. Wallis0Kenneth C. Williams1Department of Biology, Boston College, Chestnut Hill, MA 02467, USADepartment of Biology, Boston College, Chestnut Hill, MA 02467, USABefore the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive disorders, lung and kidney disease, and malignancies. The broad evidence suggests that HIV with ART is associated with accentuated aging, and that the age-related comorbidities occur earlier, due in part to chronic immune activation, co-infections, and possibly the effects of ART alone. Normally the immune system undergoes alterations of lymphocyte and monocyte populations with aging, that include diminished naïve T- and B-lymphocyte numbers, a reliance on memory lymphocytes, and a skewed production of myeloid cells leading to age-related inflammation, termed “inflamm-aging”. Specifically, absolute numbers and relative proportions of monocytes and monocyte subpopulations are skewed with age along with myeloid mitochondrial dysfunction, resulting in increased accumulation of reactive oxygen species (ROS). Additionally, an increase in biomarkers of myeloid activation (IL-6, sCD14, and sCD163) occurs with chronic HIV infection and with age, and may contribute to immunosenescence. Chronic HIV infection accelerates aging; meanwhile, ART treatment may slow age-related acceleration, but is not sufficient to stop aging or age-related comorbidities. Overall, a better understanding of the mechanisms behind accentuated aging with HIV and the effects of myeloid activation and turnover is needed for future therapies.https://www.mdpi.com/1999-4915/14/2/409HIV/SIVagingmonocytesmacrophageinflamm-aging
spellingShingle Zoey K. Wallis
Kenneth C. Williams
Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
Viruses
HIV/SIV
aging
monocytes
macrophage
inflamm-aging
title Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
title_full Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
title_fullStr Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
title_full_unstemmed Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
title_short Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging
title_sort monocytes in hiv and siv infection and aging implications for inflamm aging and accelerated aging
topic HIV/SIV
aging
monocytes
macrophage
inflamm-aging
url https://www.mdpi.com/1999-4915/14/2/409
work_keys_str_mv AT zoeykwallis monocytesinhivandsivinfectionandagingimplicationsforinflammagingandacceleratedaging
AT kennethcwilliams monocytesinhivandsivinfectionandagingimplicationsforinflammagingandacceleratedaging